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TrisexualPuppy writes "A team of scientists at Boston University has created a cure for the Ebola virus, first discovered in 1976. After setting the correct dosages, all monkeys tested with the vaccine survived with only mild effects. No tests have been performed on humans yet, as outbreaks happen infrequently and are difficult to track. Quoting NPR: '[The drug] contains snippets of RNA derived from three of the virus's seven genes. That "payload" is packaged in protective packets of nucleic acid and fat molecules. These little stealth missiles attach to the Ebola virus's replication machinery, "silencing" the genes from which they were derived. That prevents the virus from making more viruses.'"

Exactly. I talked with one of my contacts at the Atlanta CDC about this. She said that little was said at that point about exactly how they procured this method, but it is something possible only with new technologies that have evolved in the past decade. That, and the limited amount of manpower dedicated to such a project mean that unless you're really lucky, it's going to take the full 30 years.

I wonder how many lives will eventually be saved and what awards will be gotten because of this.

I can't imagine the fallout that would occur if an ebola victim went to a major international airport. It'd be horrific, and even if, as in previous cases, the ebola virus "burned out" fast, it could be an international crisis.

There, you're realistically describing an airborne version of such a virus, not an STD, and probably not even the multiple bodily fluids borne version that is the baseline Ebola virus. An STD is really a disease that spreads so poorly only direct membrane to bodily fluid contact tends to spread it. STDs typically won't spread dry skin to dry skin, or by fluids if those are exposed to sunlight or cold for even a few minutes, and they die very, very quickly if exposed to many common environmental stressors ot

One could only imagine an ebola like venereal disease. AIDS with a 90% death rate and a two week period from infection to death.

That sounds frightening- and I'm sure it would be if you actually caught it- but it would quite likely be self-limiting since people would probably die before they were likely to spread it to many- if any- other partners (two week max. window, reduced by period they were visibly ill during), and the trail of infected people would be clear- unlike "normal" AIDS where the delay of symptoms over years could make that *much* less obvious.

It's been said that ebola's aggressiveness in killing people quickly an

It is indeed a self-limiting disease, and thus not on everyone's priority list, but if the summary is correct, this is great news not only because it prevents an extremely deadly disease, but because it may give insight into combating RNA viruses as a whole, historically a difficult problem.

Further to your point, this treatment is heavily dependent on PCR (polymerase chain reaction) techniques, which are very much a stock-in-trade tool of molecular biology now, but has only been technically possible since (IIRC) 1976 when the DNA polymerase from Thermophilus aquaticus was first isolated. The components required for the reactions were available by about 1980, and I think the first automatic machines became available in about '83 or '84.

It wasn't until 2001 that RNAi was demonstrated in mammalian cells, so its use as a standard tool in molecular biology only dates back to the last decade. To apply this sort of strategy to Ebola also requires knowledge of its genome sequence, which also wasn't complete until the 90s, as well as an effective method of getting the active molecules into infected cells (like the lipid-based packaging approach used here). There is indeed active research aimed at applying RNAi to other viruses, including HIV, but it's far from straightforward.

Also, the people that will need the drug have little or no ability to pay for it. It takes A LOT of money to get a drug approved, if the market for the drug itself is not there then the work just does not get done. The technique used will be applied to other, more profitable issues, so some good comes of it in the end.It might be worthwhile to give drug companies a tax break for donating information that leads to effective cures for less profitable conditions... I'm sure there are many substances that have

the people that will need the drug have little or no ability to pay for it. It takes A LOT of money to get a drug approved, if the market for the drug itself is not there then the work just does not get done

This is also an issue for people who can pay for a drug, even United States citizens who have health insurance. There have been recent news articles highlighting the fact that the United States is facing a shortage of various anti-venoms [popularmechanics.com] because corporations are either stopping production or never bother

It might be worthwhile to give drug companies a tax break for donating information that leads to effective cures for less profitable conditions

This is an excellent idea but I would even go so far as to suggest taking out the "leads to effective cures" requirement as it can take a long time to reap the benefits and corporations would be more likely to utilize the offer if it provided an immediate tax benefit.

While I agree that this would greatly increase the incentive, I think that companies would then donate floods of information that they knew or suspected would in the end prove unproductive... because they reap an immediate benefit and that looks good on the quarterlies... If I have a dog, I expect it to act true to it's nature (i.e. "like a dog"). You can pretty much count on corporations to behave in a corporate manner. Maybe a structured schedule of small breaks for information and later "bonus" benefits

It takes A LOT of money to get a drug approved, if the market for the drug itself is not there then the work just does not get done.

That raises a question: should cures for illnesses with nearly 100% kill ratio be held to the same standards as cures for illnesses that are unlikely to kill you? After all, if the drug is guaranteed to kill the virus, then as long as it's less likely to kill you than the virus is it's in your best interests to take it. In the case of Ebola, drugs with mortality rates less 50%

I'm fairly sure I thought of it quite soon after I first learned how a virus works, in the same way that people thought of making a machine that works like a bird thousands of years ago. The step between thinking of what to do and doing it is huge. In this case, even the step between thinking of how to do it and actually doing it is pretty large.

Thought of? Sure, it's probably been thought of many times by people in the field. But having the technical ability to make it happen for real, that's new. There's several parts to that too, such as the ability to analyze the virus at that level (not been around very long, expensive but not as costly as it used to be), the ability to figure out what bits to interfere with where the virus will find it difficult to mutate and yet which won't harm the host (hard!) and the ability to manufacture and deliver th

Yes, but the ones that fail animal trials don't make it to human trials. Also, this particular drug targets the disease itself, as opposed to anything in the host; it's not a cancer treatment or anything like that. There is a respectable chance that it could work successfully in human beings. Even if it does not, it is one hundred percent successful. Completely and utterly successful. Whether it works in humans or not it'll open up new avenues of research.

You off a Howler monkey during a test you just need to do your report (necropsy ect) and get another monkey

Off a human during a test and you have1 a much larger report2 a very detailed autopsy3 a report to Legal to make sure your "assets" are covered4 a possible lawsuit from the next of kin5 it gets a bit harder to get more humans when you have a track record of offing your volunteers

OK, you've just said something that is nearly 100% true, but has almost no meaning outside of the context you've left out. RNA mutates just as DNA does, and is subject to selection in theory. So, an RNA based virus can evolve. But, there are important differences. 1. Just about every gene in a virus is vital, as that same evolutionary pressure selects to weed out all the junk code at a much higher rate. The penalties a virus pays for hauling any gene not vitally needed are so big, it ha

Viruses don't really have a lifespan. Ebola is short-lived because it's so deadly. While resistance generally does make a virus/bacteria/parasite less effective overall (resistance comes at a cost), random mutations will do the same a lot more quickly. Apparently that's not a successful strategy for the virus.

That said, if we manage to keep people from dying but not keep them from spreading the virus then that would be bad. Obviously, to get these antivirals, you're already in the quarantine. Unlike

It sounds similar to Phage Therapy [wikipedia.org], long story short you have to identify and isolate the virus in question before you can treat it, because there are so many variants of most viruses you need tons of phages to treat what we the masses think of as a single virus. If Ebola doesn't change too much, or if they found critical parts of Ebola that never change between variants, it might be possible to attack those, but targeted approaches don't work against disparate viruses.

It sounds similar to Phage Therapy [wikipedia.org], long story short you have to identify and isolate the virus in question before you can treat it, because there are so many variants of most viruses you need tons of phages to treat what we the masses think of as a single virus. If Ebola doesn't change too much, or if they found critical parts of Ebola that never change between variants, it might be possible to attack those, but targeted approaches don't work against disparate viruses.

What if one day we'll be able to synthesize a therapy while the patient is waiting in the waiting room? Just consider the leaps in DNA sequencing. Once a tedious manual process where we were lucky to decipher a few dozen nucleotides in a row, now a technology with the prospect of sequencing a person's whole DNA for a few dozen bucks. (I admit that I'm not aware of the precise state of the art today.) A century from now - if our civilization won't collapse in the meantime - we might be able to synthesize a v

Sequencing a virus ought to cost dramatically less, but first you have to identify the culprit. So while antibiotics and antivirals are only effective some of the time, any asshole can cycle through 'em until they find something that works, without having to know what illness is responsible... most of the time. Phage therapy requires that every doctor be highly skilled, which would be nice.

What if one day we'll be able to synthesize a therapy while the patient is waiting in the waiting room?

The problem is the wide variation in viruses even within a single host. Even if you can synthesize a therapy against the most common form in a host, those that are not suppressed will take dominance (as with any drug resistance). The ideal solution, and what will hopefully happen in the future, is the ability to initiate therapy with multiple target drugs to effectively corner the virus out of viability -

The method with which the "drug" works is called RNA intereference [wikipedia.org]. RNAi is more or less a standard method in molecular laboratories. Unfortunately, the efficacy of RNAi in different cells and for different proteins varies a lot, for reasons that are poorly understood. Further, RNA is rather unstable in water, and delivering substantial doses of RNA to cells in an organism has remainded challenging.

Morever, all viruses do not start with an RNA-based genome. Some DNA based viruses use promoters for their genes that cause very strong expression of the genes, like the CMV promoter [PDF alert] [wjgnet.com], which is used in isolation to create "over expression" in molecular biology. RNAi is typically very poor against such strong promoters.

Ebola is a virus that is relatively slow replicating in the initial stages. It is not a particularly ingenious design as compared to say the flu virus. This gives the RNAi a chance to work against it.

In short, I don't want to say _never_ (that'll just be ignorant), but as yet, RNAi needs a lot of research and is perhaps not the best strategy for all viruses.

Viruses that integrate into the genome of host cells would likely not be removed by this mechanism. It may be possible to inhibit the virus enough to prevent spread between cells, but persistence down cell lineages may mean lifetime treatment is required. That said, if we can suppress replication enough to prevent onward transmission eradication would be the result.

Before you start declaring a CURE!!! look at the number of test subjects. Preventing death in five monkeys is not exactly a cure. It's a very promising start, but they need to test it in non-infected humans to make sure it's not going to cause some odd problems and to get max dosages worked out.

Ebola's death rate is so high that this treatment would have to be extremely dangerous to keep it form being used. Death rates are in the 80-90% range now, so if it dropped them to even just 50% it's worth a large risk.

Um, do the maths. 100% effective in five monkeys scales out to 100% effective in 5 million monkeys in my arithmetic book. But then again my books are published in Texas....

This is a standard EE/CS/engineering view where everything is deterministic, or very nearly so.

As an EE-turned-biologist, one of the big things I had to get my head around is that like it or not, Biology is messy. Very messy. Whereas in Engineering, models that are accurate to 1% are considered adequate, and 0.1% good, in Biology, models that are accurate to merely 50% are considered good, and above that is excellent. Biology is messy. There are many, many, many uncontrolled variables, most of which are

A mortality rate of 80% of out 5 monkeys, 4 would have died. If 0 died in the vaccine group, it is a pretty significant finding.

Maybe someone here can be bothered to draw up the exact significance, but I'm pretty sure it will be a percentage surprisingly high for a sample of 5 individuals, since the mortality is so high to begin with.

For example with rabies, the mortality rate is a solid 100%. Managing to save even 1 infected individual is nothing short of a monumental achievement, as in all recorded history, we only have 3 survivors total, with Jeanna Giese being the first and the 2 others with the course derived from her treatment. - http://en.wikipedia.org/wiki/Milwaukee_protocol [wikipedia.org] - so these 3 survivor make up a pretty high significance when compared to 0 before.

The p-value is 0.00032 by my off-the-cuff calculation (pbinom(0, 5, 0.8) in R.) So yeah, it's pretty significant. That being said, sample sizes this small still do tend to make people nervous -- the p-value is calculated assuming that the monkeys in question represent a good sample of the population, and doesn't account for lab-specific or family-specific effects. (Where were the monkeys bred? How closely are they related? What sub-population do they belong to? Etc.) So we can certainly accept the finding for what it is, but regulatory bodies will, with good reason, want to see larger animal trials before approving even limited human use.

Thanks for the calculation, you are of course right with the small population that is quite possible not really representative for all genotypes. Nonetheless, it's quite good against a deadly virus like this.

My concern would be, "[The drug] contains snippets of RNA derived from three of the virus's seven genes," but how stable are those genes? The reason the flu virus often doesn't help is because there are so many different strains, they can't all be targeted at once with today's technology. You have to guess a year ahead of time which to target.

but regulatory bodies will, with good reason, want to see larger animal trials before approving even limited human use.

With all due respect, fuck *that* and fuck *them*. The mortality rate of Ebola is very high and it is very fast acting. Minutes could literally make a difference in treatment.

Considering the circumstances of finding somebody infected with Ebola and having a reasonable window for treatment I simply can't imagine a situation in which testing anything experimental was not the right thing to

I partially agree with you; I was a medic long I was a biostatistician, and in situations where the alternative to treatment -- any treatment -- is death, it's hard to argue for holding back.

The thing is, what you say about the speed with which Ebola acts is exactly right, and it's a big part of the problem with any treatment for it. Are we supposed to manufacture large stocks of the medication, distribute it to areas where Ebola is prevalent, and take whatever measures are necessary to store it and train

the weird thing is that every time the control monkey died.
* The third one died, as did a control animal that didn't get the drug
* The untreated control animal died.
so basicly the drug works a 100% on monkeys, only though when the drug is administrated, on a monkey which isn't infected it dies,..?

Before you start declaring a CURE!!! look at the number of test subjects. Preventing death in five monkeys is not exactly a cure.

It was for those 5 monkeys. Yes it does not mean it would be 100% effective in 20,000 monkeys or 1 human but it's a hell of a start. But you're right about the story summary being sensationalist. What do you expect here though?

At 85% mortality, the chance of all five monkeys surviving due to random chance would only be 15% ^ 5 = 0.0076%, which is well below the traditional alpha level of 5%. It'd take a mortality rate of 45% before you could say that, so for deadly diseases you don't need huge sample sizes to show effectiveness, though you would need a larger sample size to measure the size of the effect. The researchers have a very good claim that the treatment lowers the mortality rate of the tested strain of Ebola in monkeys

Viruses and disease is a way for mother nature to keep the balance of life, by taking this away we risk the possibility of killing off our species even faster. I only hope that I live long enough to watch 90% of the human population die because of our stupidity even though I may die as well it will be epic...

Actually, this is more of a cure and definitely a form of genetic therapy (although the genetic material isn't incorporated into the patient's genome). The scientists used RNAi in which sequences of RNA complementary to the viral RNA are injected into the patient. When the complementary sequences bind together, they activate innate cellular defenses [wikipedia.org] against double stranded RNA which destroy the genetic material, thus preventing the virus from replicating within the cell. If

How soon after you get infected would this treatment have to start? Also how soon into an ebola infection can you figure out it's ebola? Basically I'm wondering that because the scientists doing these tests know what the Monkeys are infected and can start anytime they want. I'd think delaying the treatment because of the diagnosis process would probably change the results.

The scientists behind the study are actually curious about the same thing:

Of course, in the real world, people infected with Ebola might not get the drug within 30 minutes of infection like these monkeys did. So Geisbert is planning another set of experiments.
"Can we go 24 hours or 48 hours or 72 hours before we start treatment?" he wondered. "Can we increase the window and still achieve 100 percent protection?"

Personally, I find this fascinating and I'd be interested to see the results of their next experiments as well.

Correct me if I am wrong but one of Ebola's nasty features is its ability to mutate efficiently to offset its achilles heel. It's achilles heel is that it tends to kills its victims too quickly to adequately reproduce and spread itself. This might be why outbreaks are not long lasting but are particularly lethal.

It can't be killing everything it infects quickly. Otherwise it would be extinct. What happens is it doesn't kill some animals/victims, they might get sick or be asymptomatic, and these carry it around. Current theory is fruit bats are one of the carriers.

The same unmutated strain could keep on killing say 80% of humans who are exposed, so there is no pressure to mutate from there. Whether it mutates fast or not thus would depend more on the main carriers.

The reported overall survival probability for an Ebola patient is supposedly 10%. But how many people/animals naturally have an immunity to Ebola, therefore they got infected but had no symptoms, therefore they never knew it? Then the marginal probability of surviving an Ebola infection may be greater than 10%.

Also, the survival probability changes over time depending on how long they were infected. An Ebola patient who has already survived, say, 5 days is more like

The poster is wrong to refer to the drug as a "vaccine". A vaccine works by stimulating the body's immune system to develop antibodies against the disease. This drug works by attacking the disease directly.

An unfortunate side effect was it made the monkeys very very angry and aggressive. Monkeys infected with this "Rage" are not to be approached, and if you are bitten a level 9 quarantine should be immediately put into effect. Currently the monkeys are being held in a minimum security facility "Econo-Labs" which is located right next door to Peta National headquarters. We will try making the monkeys watch FOX news, mostly because we are a bunch of dicks...